In a previous study (Gitlin et al. Cardiovascular Res., 73:227, 2007), we reported the involvement of COX-2 in the formation of abdominal aortic aneurysms (AAAs). Furthermore, preliminary studies in our laboratory have indicated that B-arrestin2-mediated signaling leads to the induction of COX-2. In the present research, we have continued these studies and investigated the roles of B-arrestin2 and COX-2 in the formation of AAAs. AAA formation involves an abnormal dilation of the aorta, followed by macrophage infiltration and extensive remodeling of the vessel wall, which with time may lead to life-threatening AAA rupture. We have used a model of angiotensin II (AngII) induced AAAs in mice to study AAA formation and investigate the roles of B-arrestin2 and COX-2 in the induction of AAAs. We previously demonstrated that the deficiency of COX-2 attenuates the incidence AAAs in mice (Gitlin et al.), and furthermore that AngII induces significant COX-2 expression in the abdominal aortas of mice. Similar to our previous observation that COX-2-deficiency reduced AAA formation, our current studies show that the deficiency of B-arrestin2 significantly reduced AngII-induced AAA formation in mice. To identify possible mechanisms by which B-arrestin2 contributes to AAA formation, we have compared the induction of COX-2, ERK1/2 activation, MCP-1 and MIP1 in B-arrestin2+/+ and -/- mice. Our conclusion is that the deficiency of B-arrestin2 attenuates the incidence of AngII-induced AAAs by decreasing B-arrestin2-mediated ERK1/2 activation and the induction of COX-2. Carbon nanotubes (CNTs) are engineered graphene cylinders that have numerous potential applications in engineering, electronics and medicine. However, a growing body of evidence indicates that CNTs cause inflammation and fibrosis in the rodent lung and suggests that these nanomaterials could pose a potential health risk. In order to elucidate mechanisms of inflammation and fibrosis caused by CNTs, we determined whether multi-walled CNTs (MWCNT) induced the differential expression of the inflammatory mediators, IL-5, IL-13 and IL-17A in the lungs of wild type and COX-2 deficient mice. The data indicated that MWCNTs induced airway inflammation was exacerbated by deficiency of COX-2 with differential activation of Th1 and Th2 immune responses. In a third project studying the role of COX-1/COX-2 in physiology/pathophysiology, in collaboration with Dr. Graham Wagner, Western University, London Ontario, we demonstrated that COX-2, but not COX-1, played a role in renal stanniocalcin-1 induction in response to dehydration.